drugs for heart failure Flashcards
heart failure
heart is unable to pump sufficient blood to meet needs of body
- systolic dysfunction
- diastolic dysfunction
consequences of heart failure
heart failure
- dec CO
- inc in sympathetic activation and dec in bp
- dec renal blood flow
- inc renin, ang II, aldosterone
- inc Na+ and water retention
- oedema
OR
- inc venous pressure
- dec glomerular filtration rate
- oedema
Name the drugs for HF treatment
- beta blockers
- sacubitril-valsasrtan
- hydralazine
- cardiac glycoside: digitalis
- diuretics
- ivabradine
- isosorbide dinitrate
beta blockers
B1 SELECTIVE
1. bisoprolol
2. metoprolol XL
NON SELECTIVE
1. carvediol
MIXED
2. nebivolol (low dose b selective; high dose non selective)
sacubitril- valsartan MOA
- neprilysin inhibitor + AT1 blocker (ARNI)
- inhibit BNP breakdown by neprilysin : prolonged BNP effects
- inhibit ang II effects by blocking ang II receptors
- natriuretic peptide system: activated under HF
- brain natriuretic peptide BNP increases
- BNP promotes vasodilation, natriuresis, diuresis
- BNP antagonises RAAS (prevent vasoconstriction, decrease afterload)
=> favourable effects
Why is valsartan needed in combi with sacubitril?
sacrubitril inhibits neprilysin
neprilysin breaks down ang II
=> prolonged ang II effects
valsartan needed to block ang II effects
sacubitril-valsartan adverse effects
- hypotension
- hyperkalaemia
- renal failiure
- cough
- angioedema
hydralazine MOA
- direct arteriole vasodilator
- inhibit IP3 calcium release from smooth muscle cells sacroplasmic reticulum
- reduce peripheral resistance-> compensatory release of NA/A
- inc venous return and CO
hydralazine clinical uses
- heart failure with reduced ejection (given w ISDN)
- 2nd line antihypertensive
- acute post partum HTN
hydralazine adverse effects
- flushing
- hypotension
- tachycardia
baroreflex associated sympathetic activation
hydralazine route of administration
IV: onset 5-30 min
oral: onset 20-30 min
7h half life
digitalis MOA
- digitalis inhibit Na K ATPase exchange
- increase [Na+] as it cannot exit cell
- leads to decrease in Ca2+ efflux at the Na Ca exchange
- increase intracellular Ca2+
- increase systolic contraction
digitalis clinical use
- systolic dysfunction
- atrial fibrillation
digitalis adverse effects
- GI disturbance: nausea vomiting
- CNS: headache fatigue
- dysrhythmia: AF VF AV block
Name a commonly used digitalis
a type of cardiac glycoside
DIGOXIN
Digitalis toxicity treatment
- stop cardiac glycoside treatment
- antiarrythmatic drugs
- correction of magnesium and potassium deficiency
- digitalis antibody
isosorbide mononitrate/ dinitrate moa
vasorelax-> arteriole and venous dilation -> dec in afterload and preload
-> CO and bp decreases-> therapy of CHF
Loop diuretics (furosemide) MOA
- inhibit Na+/K+/2Cl- transporter in the thick ascending limb of Loop of Henle
- inhibit reabsorption of Na+, K+ Cl-, increase diuresis (urine production)
- induce renal prostaglandin synthesis -> vasodilation, inc renal blood flow
very fast onset
loop diuretics clinical uses
- oedema
- hyperkalemia
- acute renal failure
- anion overdose
loop diuretics adverse effect
- hypokalemic metabolic alkalosis
(dont use with aminoglyvoside) - ototoxicity
- hyperuricemia
- hypomagnesemia
potassium sparing diuretics MOA
promote diuresis without loss of K+
1. aldosterone receptor blockers decreased Na+ and H2O retention: spironolactone, eplerenone
- Na+ channel blockers, decrease reabsorption of Na+ hence excretion of K+: amiloride, triamterene
very slow onset
potassium sparing diuretics clinical uses
- diuretic
- hyperaldosteronism
potassium sparing diuretics adverse effects
- hyperkalemia
- acute renal failure
- metabolic acidosis
- kidney stones
